Weight loss and Toxic

March 14, 2014

Weight loss and Toxic-Need to detoxify

When making effort to lose weight, you may choose to look at your toxic level and try natural means

Many people are struggling with weight and obesity in the today’s society, in order for your body to lose weight, there must be adequate hormones insulin and leptin must be doing their work. Insulin is in place to control sugar and fat storage levels in the body while leptins job is the burning of fat. If these hormones and the mechanisms that are there to utilize them isn’t working, you will be unable to lose weight and extremely prone to packing it on. There are two reasons these hormones begin to fail in your body, the over-consumption of sugar and processed grains and toxicity.

Toxicity is perhaps the greatest problem in the fight to lose weight. When toxins enter your body they have an affinity for fat cells, due to the fact that they are fat soluble. When the toxins attach to the outer cell membrane which is made of a lipid bi-layer (two layers of fat), it causes the cells to continually release Leptin which is the hormone that tells the brain to burn fat for energy, therefore, weight gain that does not respond to exercise or diet is inevitably due to Leptin resistance.

The toxins also cause the release of chemicals called cytokines that damage Leptin receptors in the brain (hypothalamus). Once the receptors to Leptin have been damaged, Weight Loss becomes a problem your body then makes an extremely important hormone called MSH (Melanocyte Stimulating Hormone). MSH is produced in the hypothalamus by Leptin, and it controls nerve, hormone, cytokine functions, skin and mucus membrane defenses, as well as controls the production of endorphins and melatonin. If your brain cannot hear Leptin you will eventually become MSH deficient. The effect of this would be that every immune and hormone response in your body will be altered. This then leads to so many different diseases like depression, diabetes, cancer, heart disease, chronic fatigue, and fibro-myalgia, just to name a few.

In many ways, our polluted world is a true test of genetic survival of the fittest. The number of toxic chemicals now threatens the reproductive ability of the human race and is also a large part of the cancer issue. These chemicals contribute to weight gain in various ways, including disruption of the hormone signaling system that regulates your metabolism, damage to and accumulation in your white adipose tissue, and increased risk for poisoning during weight loss. It is absolutely vital that you understand this subject.

Weight loss and Toxic-Challenges

It is very clear that too toxins are released back into the circulation during weight loss. This is especially the case during significant weight loss. During a weight loss of 12 percent of body weight toxins in the blood increased 23 percent – 51 percent, with the heaviest individuals releasing the most toxins. Over a one year period of weight loss toxic exposure ranged up to a whopping 388 percent. Scientists have shown that such toxins can interfere with thyroid hormone function during weight loss. Human data shows that as the toxins go up in the blood during weight loss the levels of biologically active thyroid hormone (T3) go down. This data means that your plumbing and detoxification systems must be in good working condition for healthy weight loss or possibly even to engage weight loss.

Toxins make you feel irritable. Many people report feeling poisoned at a certain point in their weight loss process. Such people will always feel better when they eat a lot of food, as the toxins are pulled out of their blood and placed back in fat along with plenty of fat. With little effort, most people can readily lose weight they have most recently gained. After that, people reach what I will call the “toxic plateau.” This means that detoxification strategies may need to be adjusted if weight loss slows too much or stops.

Weight loss and Toxic-Toxic Environment

Once upon a time, the Environmental Protection Agency (EPA) conducted a program called the National Human Adipose Tissue Survey (NHATS). In 1982 and again in 1987 it analyzed human fat samples from cadavers obtained throughout the country, looking for the types of toxins that accumulate in human fat. Four industrial solvents and one dioxin were found in 100 percent of the fat samples. Nine more chemicals, including three more dioxins and one furan were found in more than 90 percent of the fat samples. In general, 83 percent of the fat samples contained PCBs. U.S. researchers have confirmed the presence of multiple toxins in human fat associated with obesity risk. The EPA has confirmed the presence of these chemicals as pollution in the farm soil across America this can only mean that this problem will be with us for some time to come.

The scientific theory of how these chemicals cause weight gain and difficulty losing weight has now been established. They bind to gene signaling within white adipose tissue and induce new fat cells to form while simultaneously increasing inflammation. Oftentimes, the newly formed fat cells are themselves damaged by the toxins so that they cannot metabolically perform, which includes an inability to make leptin normally. These damaged fat cells can fill up with excess fat and toxins, but are not able to efficiently carry out normal functions of fat cells, leading directly to increased risk for type 2 diabetes via the suppression of the important fat cell hormone known as adiponectin. Several human studies confirm that PCBs increase diabetes risk. These chemicals pose a serious problem to the thyroid gland and the efficient utilization of thyroid hormone throughout your body.

Weight loss and Toxic-Strategies detoxification during Weight Loss

The steps to take to boost antioxidant nutrients that are known to help detoxification processes while protecting the liver, brain, white adipose tissue, and/or circulation. Top choices are silymarin, R-alpha lipoic acid, chlorella, quercetin, grape seed extract and tocotrienols. It is now understood that “toxic” blood triggers the formation of new fat cells. This is because the endothelial cells of your circulatory system directly communicate to your baby fat cells and can tell them what to do. Keeping your blood as clean as possible and supporting your liver are vital steps to ensure that this process goes smoothly. While making all these efforts a decision to visit AWAREmed Health and Wellness Resource Center under Doctor Akoury’s who cares a lot will make great difference here we focus on Neuroendocrine Restoration (NER) to reinstate normality through realization of the oneness of Spirit, Mind, and Body, Unifying the threesome into ONE.

Weight loss and Toxic-Need to detoxify

Social and health consequences of cocaine use

March 13, 2014

Social and health consequences of cocaine use-Addiction

Social and health consequences of cocaine use-Everyone is affected

The use of cocaine has negative effects on the society

Almost on a daily basis on my way to my work place I pass a small park on the way. In this park and along the road a group of people is sitting, standing or lying down with bottles of wine in their hands or tins with beer. They are not very good looking and not presentable at all, sometimes they show up in rags and some have hairdos that look like a Zoo. They seem engaged in quite energetic talking but at the same time some sit listening quietly and some even seem to sleep.

This group is a group of street drinkers. They all know each other and their place of congregation is the little park. Quite clearly they have no jobs, at least not at the time I meet them socializing, majority of them are men.

On the other hand at my work place I have a different experience I talk to another group of people usually very well dressed people in a nice room, during lunch, dinner or at the occasion reception. A reception will be created when for instance someone says good bye as a professor and goes to another university. Also we have receptions after a doctoral thesis has been defended. During these receptions people stand and almost all have glasses in their hands, filled with red wine, white wine or sometimes even stronger drinks like gin or whiskey. People laugh, have energetic discussions or wander quietly from person to person. All of these people have jobs. They are both men and women, in almost equal proportions well-mannered and dressed sophistically.

Looking at these two groups observations serve as lesson. Tow lessons one in the sociology of drug use. The common drug that played a role in the two described situations was of course alcohol, hence the topic of my presentation in this, Cocaine use and its social and health consequences, will be modeled along the structure that these two situations allow me to create.

Cocaine users can be found in poor ghettos of cities of the world, but also in the suburbs or rich dwellings. But in our own cocaine user studies we found crack cocaine users among well employed highly functional completely integrated cocaine users. How then are we going to approach the question what health and social consequences cocaine use can have?

Lesson number two. We have to be prepared that a simple answer to this question does not exist. Quite clearly, as is the case in the two groups of alcohol users I started to describe, we should be ready to accept that the answers to the question may be very different from one kind of cocaine user to the next. Very much depends two things (1) on the group to which the user belongs and (2) the use patterns of the user.

In groups where unemployment is the rule, criminal behavior as well, poor housing conditions prevail and where social integration into dominant labour or family culture is low, the user of cocaine, or of alcohol, or of whatever drug will behave very differently from when the user is part of another sub culture. If you do not go to work, why would you stop using cocaine at 9 o’clock at night? If you do not have to impress your boss every morning by looking brilliant, the contextual restraints on your time management are really different than when you have.

If you are not part of a culture in which you eat every day, and eat well, the health consequences of alcohol, but also of cocaine, will be different than when you eat well and regularly. If you smoke cocaine to escape constantly some sort of social misery, the effect you seek are different from when you smoke cocaine to take off on an adventure of sexuality and excess.

Apparently people seek effects that they sometimes get from drugs, and try to get those effects again. The type of drug effects people seek can be very different, even with the same drug. The two types of alcohol users I introduced to you in the beginning, are seeking different types of effects from alcohol. The choice of effects depends very much on your social home, but also on your character and the interplay between situation and moods.

Social and health consequences of cocaine use-Scores of Variables

With alcohol we all know a typical kind of user, who will consume some alcohol every day, but in low amounts and to very low or even zero levels of intoxication. They visit a bar after work or have a drink at home while chatting with kids. One could give such a use pattern a name, like frequent use zero intoxication. This is a very neutral type of name. Another possibility is that a daily wine user, who chooses the wine very carefully to match the chosen food of the day, but not as a vehicle for intoxication, could be named as a gourmet alcohol user. The same is true for cocaine, although with cocaine users taste can be important, but in a very different way as for a wine user. A cocaine user will appreciate the mellow bitter taste, or the subtle freeze in the back of the tongue.

We have found a substantial proportion of cocaine users who would use the substance every day but with very little amounts, less than 0.5 gram a week, who like to experience the freeze, or the very mild post dinner stimulation, very much like people who have coffee after dinner. For this they need very small lines of cocaine, even if their wealth or available stock of cocaine in their office drawer would allow much greater quantities of use.

Social and health consequences of cocaine use-The story of the consequences

Looking at pattern of use plus looking at social or cultural group a user belongs; one can see distinct types of cocaine use where the social and health consequences are almost zero. If cocaine use does not interfere with eating, if it does not interfere with social functioning both in the inner group as in relation to outside groups the social consequences are nil.

However, it is possible to identify daily users of cocaine, where the amount of use is higher or very high, and where the level of intoxication is desired to be high, and where the user’s group is willing to create the social background for this type of frequent high intensity use. Here the social consequences will be small in the primary group to which the user belongs, but quite dramatically negative in relation to outside groups.

But we can see with alcohol, as with cocaine that some users will use to excess, or consume so much to support a particular behavior or emotional effect that even the inner group is not going to accept this. If this happens, as will occur with some users, the social consequences are severe. Heavy consumers will find themselves with deeply disturbed social relations, sometimes resulting in complete ostracism and even death. Quite probably these rare use patterns are driven by complex problems that justify the choice of these patterns although ultimately they may prove to be very counterproductive. Most often, such extreme use patterns are left behind as soon as the user finds some possibility of more useful adaptation.

However, also quite destructive social consequences can happen to a consumer of cocaine who has no conspicuous use pattern at all. Imagine someone who lives the life of a highly valued and well known adviser to the Minister of Health. However, in her free time she invites artists and actors to her very nice flat on the river side. Cocaine is snorted and one of the elderly guests makes a mistake, snorts too much cocaine on top of his whiskey and has a heart attack. The guest is taken to the hospital and fortunately survives, but the story is out and in the papers. You can avoid this by visiting AWAREmed Health and Wellness Resource Center under Doctor Akoury for help on addiction. They focus on Neuroendocrine Restoration (NER) to reinstate normality through realization of the oneness of Spirit, Mind, and Body, Unifying the threesome into ONE.

Social and health consequences of cocaine use-Addiction

Obesity and sugar addiction

March 13, 2014

Obesity and sugar addiction-Neuroendocrine imbalances

Obesity and sugar addiction-Sugar, sweetness or palatability

Sugar addiction is associated with obesity what you eat can have diverse effect on your life.

The concept of sugar addiction relies on rats given the choice between a palatable sucrose solution and a much less palatable chow. Naturally in such circumstances they consume sucrose. The question is whether it is sucrose, sweetness or palatability to which they are responding? It needs to be demonstrated that similar behavior could not be demonstrated with carbohydrate in general, artificial sweeteners or fat-rich palatable foods. Comparisons have been made between the reaction of rats to the provision of sucrose, a high-fat diet and a sweet-fat combination. The ability of the opioid antagonist naloxone to produce withdrawal symptoms was not observed with fat although it occurred when sucrose alone was provided, evidence that in this paradigm different types of palatable food produce different responses.

However, it appears that rats do not have a preference for sucrose consumption as there is a preference for sucrose in sham feeding studies, where after passing through the mouth it leaves the body, ensuring no post-ingestive effects occur. Dopamine is released from the nucleus accumbency with this procedure. The sweetness of fruit juices is rewarding as judged by “reward expectation-related neuronal activity” in the primate striatum, although it is produced by sugars other than sucrose.

There is a preference for artificial sweeteners that in turn have been shown to influence the activity of the nucleus accumbency. The intermittent access of rats to a saccharin solution rather than sucrose has also resulted in withdrawal symptoms when consumption stopped. It appears that in part at least there is a response not to sucrose but rather to a sweet taste.

More generally, is the response of a rat specifically to sweetness rather than palatability? Woolley questioned whether the opioid regulation of food consumption reflects the macronutrient content rather than flavor. They studied the consumption of two types of food pellets that differed in flavor although they were nutritionally identical. A μ-opioid receptor agonist injected into the nucleus accumbency increased the consumption of both pellets in a similar manner if they were tested when only one of the two foods was present. However, when both flavors of pellets were presented simultaneously, the agonist increased and the antagonist naltrexone selectively decreased the consumption of the preferred flavor. The authors suggested that based exclusively on flavor cues, opioid mechanisms in the nucleus accumbency increase the intake of palatable foods. Similarly the administration of naltrexone into the nucleus accumbency selectively decreased sucrose intake, although it had only a minimal influence on the consumption of less preferred chow. In addition a specific μ-agonist selectively increased the intake of sucrose, saccharin and a dilute saline solution. These findings demonstrated an important role for opioids in the nucleus accumbency in promoting the consumption of preferred palatable foods. When rats consumed a high-palatability sucrose solution the release of dopamine in the nucleus accumbency was dose dependent but palatable high-fat/sweet foods similarly induced dopamine release. The message is that it is palatability rather than sweetness or being sucrose that is critical in determining food preference.

This conclusion is supported by studying the impact of opioid drugs. As a generalization it has been known for many years that opioid agents enhance and opioid antagonists decrease feeding. In the rat the positive facial response to a sucrose solution was enhanced by morphine and decreased by opioid antagonists. The administration of morphine caused a short-term increase in food intake, and at least initially an increase in fat intake at the expense of carbohydrate.

The opioid antagonist, naloxone decreased fat rather than carbohydrate consumption in rats. As it is known that for many rats fat is more attractive than carbohydrates these finding are consistent with the view that opioid mechanisms influence the intake of palatable foods. Such a suggestion is supported by the study of initial food preferences. As there is variability amongst rats in their preferences for carbohydrate and fat Gosnell considered whether morphine was acting on food preferences. They distinguished fat-preferring from carbohydrate-preferring rats. Morphine increased carbohydrate intake in carbohydrate-preferring rats and increased fat intake in fat-preferring rats. Therefore morphine increased the intake of the preferred diet rather than a specific macronutrient. Similarly naloxone selectively decreased the intake of preferred foods and not sucrose content as would be predicted by the ‘sugar addiction’ hypothesis.

Obesity and sugar addiction-Sugar and reward mechanisms

Addictive drugs and palatable food both release dopamine from the nucleus accumbency.

The nucleus accumbency has different populations of neurons that are activated by natural and drug reinforcement. The release of dopamine by natural rewards, unlike drugs of abuse, undergoes rapid habituation.

Although the food-induced release of dopamine is markedly inhibited by pre-exposure to visual and olfactory stimuli that have been conditioned to food, similar visual and olfactory stimuli that had previously been conditioned to drugs of abuse strongly potentiate the dopaminergic reaction.

The suggestion, based on the animal evidence, is not that palatable foods are physically addictive but rather that a particular style of eating can produce a reaction to food that is similar to the response to drugs of abuse.

Obesity and sugar addiction-Comparisons of dopamine release induced by food and drugs of abuse

Although addictive drugs and palatable food both increase the release of dopamine from the nucleus accumbency it appears that they influence different populations of neurons. Such a conclusion is supported by studies in which either pharmacological manipulation or selective lesions reduce the self-administration of cocaine but do not influence the response to natural rewards. For example Caine and Koob used 6-hydroxydopamine to deplete the nucleus accumbency of dopamine and found a reduction in cocaine self-administration without altering the response to food.

Additional evidence arises from the study of the time scale of dopamine release. Dopaminergic functioning can be estimated using a range of methods. Recording the rate of firing of dopaminergic neurons allows the examination of functioning in a milli-second time frame. Similarly voltammetry measures dopamine release over sub-second periods. In contrast, microdialysis is used to estimate extra-cellular concentrations of dopamine over longer periods.

Finally research and studies will always be done on this topic obesity and addiction to find the scientific solution, nevertheless to achieve optimal weight loss in a record time efficiently and economically, it will be necessary to pay a visit to AWAREmed Health and Wellness Resource Center under Doctor Akoury’s where a lot of focus is put on Neuroendocrine Restoration (NER) to reinstate normality through realization of the oneness of Spirit, Mind, and Body, Unifying the threesome into ONE. This way you will get help fast while the endless researches and studies continue.

Obesity and sugar addiction-Neuroendocrine imbalances

Obesity and emerging neurobiology addiction

March 12, 2014

Obesity and emerging neurobiology addiction-Food addiction

Emerging neurobiology addiction offers healthy ground for obesity take a walk swim your weight away at the beaches.

It’s believed that the increased availability and consumption of highly palatable foods is the major factor behind the rise of obesity in developed countries. Many of these highly palatable foods are sweet tasting and appealing foods that contain high levels of the natural sugar sucrose. There are alternatives to sucrose the artificial sweetener sucralose is 600 times sweeter and does not contain calories but the obesity epidemic continues because the society prefers sucrose to sucralose.

Progress has been made in recent years in understanding the neurobiological underpinnings for this preference, sucrose activates dopamine neurons in a section of the brain called the striatum, and the resulting release of dopamine is associated with pleasure. Sucralose, on the other hand, does not have this effect. Moreover, the repeated consumption of high levels of sucrose can create a cycle of continued overconsumption even compulsive eating in order to recapture the initial feelings of pleasure. This is similar in many ways to drug abuse or addiction, and also involves some of the same signaling pathways within the body.

Obesity and emerging neurobiology addiction-Optogenic techniques

Researches used optogenetic techniques to show that activating dopamine neurons in the brain encouraged mice to eat in the absence of a sweet taste. The mice preferred water to sugar if their dopamine neurons were activated at the same time that they were offered the water.

A team of researchers reports that the release of dopamine is driven by melanin-concentrating hormone (MCH) neurons in the lateral hypothalamus of the brain. The experiments relied on transgenic mice in which the MCH neurons could be activated with a carefully directed light stimulus, and showed that mice preferred sucralose to sucrose when their MCH neurons had been activated. This finding was confirmed with mutant mice that lacked the cellular machinery required to recognize sweet tastes; these mice still preferred sucrose over sucralose because of its caloric content.

Researchers then engineered mice that did not have any MCH neurons at all. The fact that these mice preferred sucralose to sucrose supports a model in which MCH neurons appear to function as both a sucrose sensor and a nutrient sensor. Taken together, the results demonstrate that preference for sucrose is dependent on at least three factors: its ability to activate MCH neurons; its sweet taste as detected by the taste buds; and, as previously reported, the metabolic state of the organism. Consistent with these findings, they propose a model in which MCH neurons act as a key component of the neuronal networks that lead to the release of dopamine in response to the detection of sucrose.

Obesity and emerging neurobiology addiction-Different responses of sucrose and sucralose

A researcher showed that sucrose activates melanin-concentrating hormone (MCH) neurons in the lateral hypothalamus (LH), which leads to the release of dopamine (DA) in the striatum: pathway shown in red. In contrast, sucralose can only induce the release of dopamine if optogenetic techniques are used to activate the MCH neurons; pathway shown in green. However, it is almost certain that various other neuronal pathways (shown by black dashed lines) are involved; these might include orexin/hypocretin (OX) neurons in the lateral hypothalamus, or other neurons elsewhere in the brain.

While this latest work shows that sucrose preference is based on its nutritive value, the actual molecular mechanisms via which it affects MCH neurons remains unknown. According to one report, since sucrose contains glucose, it could modulate the excitability of MCH neurons via potassium channels that are gated by ATP.

Experts now suggest that the activation of the MCH neurons by sucrose might be mediated indirectly by afferent nerve fibers originating from taste sensors in the taste buds and/or the gastrointestinal tract. The receptors that respond to sweet tastes also respond to the nutritional content of the food and help determine which neuropeptides should be released by taste buds Moreover, sucrose, unlike sucralose, is known to act on taste receptors in the gastrointestinal tract): this modulates the release of hormones which serve to inform the brain about the availability of calories in the body)

Taken together, these data suggest that taste receptors in both the gustatory system (the part of the sensory system that responds to taste) and the gastrointestinal system may respond to natural sugars in one way and to artificial sugars in a different way.

An outstanding challenge is to find out how MCH neurons activate dopamine neurons in the striatum. One possibility is that the orexin/hypocretin neurons in the hypothalamus have a role. Since these neurons are involved in the regulation of the desire for sugar, and they are also known to interact with MCH neurons, they might work together with MCH neurons to trigger reward.

The work of researchers represents a significant advance in our understanding of the neural mechanisms underlying how mammals respond to some kinds of foods. We now understand better why we have an innate desire for sweet foods, which are highly caloric and might have been, in the past, advantageous from an evolutionary perspective. Yet in the modern world, where highly caloric food is readily available, how do we resist this drive so as to avoid the many problems that are associated with obesity?

Interestingly, it appears that the increased use of non-caloric sugar substitutes as a mechanism to prevent weight gain or enhance weight loss has come at a cost. Recent studies show that prolonged consumption of sucralose and other high-intensity sweeteners can have potentially harmful effects on energy metabolism. On the other hand, it has been reported that non-caloric sugar substitutes do little to reduce feelings of hunger.

Noting the struggle of addiction, we need to consider using new methods of treatment that will not be addictive in anyway. For the most effective Addiction Recovery is not healthy to keep using the chemical medicine, but instead to use a Natural addiction treatment to rid the victim from drug addiction. Experience a revolutionary nutritionally assisted detox program with Doctor Dalal Akoury at AWEREmed health and wellness resource centre. Here we focus on Neuroendocrine Restoration (NER) to reinstate normality through realization of the oneness of Spirit, Mind, and Body, Unifying the threesome into ONE.

Obesity and emerging neurobiology addiction-Food addiction

Lyme disease and Climate Change

March 11, 2014

Lyme disease and Climate Change-New Findings

Research has found out that Lyme disease is greatly associated with climate change.

Historically, Lyme disease is heavily present in the Northeastern United States due to its moderate climate. The feeding period of these ticks in the northeast is being prolonged due to the extended summer temperatures, allowing more time for uninfected larval ticks to become a carrier of the Lyme disease-causing bacteria. Researchers at Yale University have seen clear implications that as the planet warms, more reports of Lyme disease will be expected in the upper Midwest to match the amount of cases in the upper Northeast.

Lyme disease and Climate Change-Borrelia burgdorferi

Borrelia burgdorferi is the name of the bacteria that causes Lyme disease and the nymphal deer tick is the carrier of this pathogen, contracting it from its blood meal. When a pathogen carrying tick bites, the bacteria enters the bloodstream and the victim becomes infected

Lyme disease and Climate Change-Transportation of Lyme disease

Deer ticks have an average two year life span, with three main life stages larval, nymphal and adult. They obtain one meal consisting of blood during each main life phase in order to survive. If the source of their meal is infected with the Lyme disease-causing bacteria (Borrelia burgdorferi) then it is passed onto the tick. In the tick’s nymphal stage, it passes the infection to its next meal source human or other animal. This feeding cycle is seasonal and innately influenced by climate.

Lyme disease and Climate Change-How Lyme Enters the Food Chain

At the propagation of the larval deer tick is born it is not born as a carrier of the disease. The ticks need to obtain sustenance in order to survive; this nutrition comes in the form of a blood meal which they obtain by sucking the blood of other animals. If the larval tick gets a blood meal from a deer or in a more likely case, a mouse already carrying the disease, the larval tick is then infected with B. burgdorferi.

In order to reach the next phase of the tick’s life, the tick must obtain another blood meal in its nymphal stage, and in the feeding process the tick passes the pathogen on to its meal source, which in some cases is a human. The human will, as a result, become a host for the pathogen. Deer have been the main suspect in being the carrier of the B. burgdorferi, but research shows that this may not be the case because the deer has the ability to flush the disease out of its system. The new suspect is the white-footed mouse, whose body does not entirely dispose of the bacteria.

Lyme disease and Climate Change-What Climate Change means for Lyme disease?

Climate change will have the following effects on Lyme disease: An acceleration of the tick’s developmental cycle, a prolonged developmental cycle, increased egg production, increased population density, and a broader range of risk areas. The ideal habitat for these disease-carrying ticks is one with 85% humidity and a temperature higher than 45°F. The tick finds a suitable microclimate by using its thermo receptors.

Once the larvae have molted into the nymphal stage, the winter forces them to remain dormant until spring. An adult tick no longer needs to hibernate during the winter, so these ticks may become active on warm winter days, yielding a larger nymph population the following year. With an earlier winter thawing, nymphal-staged ticks will become active sooner. The warmer winters will also allow for a higher survival rate of the white-footed mouse, a popular host for the ticks, meaning an increased tick population in the spring and summer.

After discovering how global warming could impact on infectious disease, scientists from Yale University, in collaboration with other institutions, have determined that climate impacts the severity of Lyme disease by influencing the feeding patterns of deer ticks that carry and transmit it.

But, as the Yale team demonstrates, it’s the seasonal cycle of feeding for each stage of the tick’s life that determines the severity of infection in a given region. The researchers found that this cycle is heavily influenced by climate. In the moderate climate of the Northeastern United States, larval deer ticks feed in the late summer, long after the spring feeding of infected nymphs. This long gap between feeding times directly correlates to more cases of Lyme disease reported in the Northeast by the scientists.

When there is a longer gap, the most persistent infections are more likely to survive. These persistent bacterial strains cause more severe disease in humans, leading more people to seek medical attention and resulting in more cases.

But in the Midwest, where there are greater extremes of temperature, there is a shorter window of opportunity for tick feeding, and therefore a shorter gap between nymphal and larval feedings. Due to this, Midwestern wildlife and ticks are infected with less persistent strains, which correlates with fewer cases of Lyme disease reported in the Midwest.

The clear implication of this research is that, as the planet warms, the Upper Midwest could find itself in the same situation as the Northeast: longer gaps between nymphal and larval feeding, and therefore, stronger, more persistent strains of Lyme disease. Other diseases, like malaria, have also been projected to expand in response to climate change, but this is the first study to show how the severity of disease can also be related to climate.

Lyme disease and Climate Change-New Findings

Category Archives: Healthy Aging